ArticleBioengineered2022
Overexpression of microRNA-381-3p ameliorates hypoxia/ischemia-induced neuronal damage and microglial inflammation via regulating the C-C chemokine receptor type 2 /nuclear transcription factor-kappa B axis.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Blood-derived microRNA signatures associated with hippocampal structure and atrophy rate: findings from the Rhineland Study.Molecular psychiatry · 2026Article
- Regulatory Roles and Therapeutic Potential of miR-122-5p in Hypoxic-Ischemic Brain Injury: Comprehensive Review.Cell biochemistry and biophysics · 2025Review
- Whole Transcriptome RNA-Seq Reveals Drivers of Pathological Dysfunction in a Transgenic Model of Alzheimer's Disease.Molecular neurobiology · 2025Article
- Involvement of extracellular vesicle microRNA clusters in developing healthy and Rett syndrome brain organoids.Cellular and molecular life sciences : CMLS · 2024Article
- Seipin overexpression attenuates cerebral ischemia-reperfusion injury via preventing apoptosis and autophagy.Brain and behavior · 2023Article
- MiR-144-5p/CCL12 Signaling Axis Modulates Ischemic Preconditioning-Mediated Cardio-protection by Reducing Cell Viability, Enhancing Cell Apoptosis, Fibrosis, and Pyroptosis.Applied biochemistry and biotechnology · 2023Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
microRNAs, as small endogenous RNAs, influence umpteen sophisticated cellular biological functions regarding neurodegenerative and cerebrovascular diseases. Here, we interrogated miR-381-3p's influence on BV2 activation and neurotoxicity in ischemic and hypoxic environment. Oxygen-glucose deprivation (OGD) was adopted to induce microglial activation and HT-22 neuron damage. Quantitative polymerase chain reaction (qRT-PCR) was taken to check miR-381-3p expression in OGD-elicited BV2 cells and HT-22 neurons. It transpired that miR-381-3p expression was lowered in BV2 cells and HT-22 cells elicited by OGD. miR-381-3p up-regulation remarkably hampered inflammatory mediator expression in BV2 cells induced by OGD and weakened HT22 neuron apoptosis.
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Registered trials
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